Phospholipids have recently been found to be integral elements of hormone signalling pathways. An Arabidopsis thaliana double mutant in two type III phosphatidylinositol-4-kinases (PI4Ks), pi4kIIIβ1β2, displays a stunted rosette growth. The causal link between PI4K activity and growth is unknown. Using microarray analysis, quantitative reverse transcription polymerase chain reaction (RT-qPCR) and multiple phytohormone analysis by LC-MS we investigated the mechanism responsible for the pi4kIIIβ1β2 phenotype. The pi4kIIIβ1β2 mutant accumulated a high concentration of salicylic acid (SA), constitutively expressed SA marker genes including PR-1, and was more resistant to Pseudomonas syringae. pi4kIIIβ1β2 was crossed with SA signalling mutants eds1 and npr1 and SA biosynthesis mutant sid2 and NahG. The dwarf phenotype of pi4kIIIβ1β2 rosettes was suppressed in all four triple mutants. Whereas eds1 pi4kIIIβ1β2, sid2 pi4kIIIβ1β2 and NahG pi4kIIIβ1β2 had similar amounts of SA as the wild-type (WT), npr1pi4kIIIβ1β2 had more SA than pi4kIIIβ1β2 despite being less dwarfed. This indicates that PI4KIIIβ1 and PI4KIIIβ2 are genetically upstream of EDS1 and need functional SA biosynthesis and perception through NPR1 to express the dwarf phenotype. The slow root growth phenotype of pi4kIIIβ1β2 was not suppressed in any of the triple mutants. The pi4kIIIβ1β2 mutations together cause constitutive activation of SA signalling that is responsible for the dwarf rosette phenotype but not for the short root phenotype.
- MeSH
- 1-fosfatidylinositol-4-kinasa genetika metabolismus MeSH
- Arabidopsis anatomie a histologie enzymologie genetika růst a vývoj MeSH
- down regulace genetika MeSH
- fenotyp MeSH
- genom rostlinný MeSH
- genotyp MeSH
- kinetika MeSH
- kořeny rostlin anatomie a histologie růst a vývoj MeSH
- kyselina salicylová metabolismus MeSH
- listy rostlin genetika růst a vývoj MeSH
- metabolismus lipidů genetika MeSH
- modely genetické MeSH
- mutace genetika MeSH
- nemoci rostlin genetika imunologie mikrobiologie MeSH
- odolnost vůči nemocem genetika imunologie MeSH
- proteiny huseníčku genetika metabolismus MeSH
- Pseudomonas fyziologie MeSH
- reaktivní formy kyslíku metabolismus MeSH
- regulace genové exprese u rostlin MeSH
- signální transdukce MeSH
- upregulace genetika MeSH
- výhonky rostlin růst a vývoj MeSH
- Publikační typ
- časopisecké články MeSH
- práce podpořená grantem MeSH
Interaction of a plant with a fungal pathogen is an encounter with hundreds of molecules. In contrast to this, a single molecule often decides between the disease and resistance. In the present article, we describe the defense responses triggered by AvrLm1, an avirulence gene from a hemibiotrophic ascomycete, Leptosphaeria maculans, responsible for an incompatible interaction with Brassica napus. Using multiple hormone quantification and expression analysis of defense-related genes, we investigated signaling events in Rlm1 plants infected with two sister isolates of L. maculans differentiated by the presence or absence of AvrLm1. Infection with the isolate carrying AvrLm1 increased the biosynthesis of salicylic acid (SA) and induced expression of the SA-associated genes ICS1, WRKY70, and PR-1, a feature characteristic of responses to biotrophic pathogens and resistance gene-mediated resistance. In addition to SA-signaling elements, we also observed the induction of ASC2a, HEL, and CHI genes associated with ethylene (ET) signaling. Pharmacological experiments confirmed the positive roles of SA and ET in mediating resistance to L. maculans. The unusual cooperation of SA and ET signaling might be a response to the hemibiotrophic nature of L. maculans. Our results also demonstrate the profound difference between the natural host B. napus and the model plant Arabidopsis in their response to L. maculans infection.
- MeSH
- Ascomycota metabolismus MeSH
- Brassica napus účinky léků metabolismus mikrobiologie MeSH
- časové faktory MeSH
- ethyleny metabolismus MeSH
- fungální proteiny metabolismus farmakologie MeSH
- kyselina salicylová metabolismus MeSH
- listy rostlin účinky léků metabolismus mikrobiologie MeSH
- nemoci rostlin MeSH
- regulace genové exprese u hub MeSH
- signální transdukce fyziologie MeSH
- Publikační typ
- časopisecké články MeSH
- práce podpořená grantem MeSH
